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Microbial Modulation of the Development and Physiology of the Enteric Nervous System

期刊

TRENDS IN MICROBIOLOGY
卷 29, 期 8, 页码 686-699

出版社

CELL PRESS
DOI: 10.1016/j.tim.2020.11.007

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资金

  1. La Fondation des Treilles
  2. French Ministry of Research
  3. Universite de Lyon
  4. FRM grant [Equipe FRM DEQ20180339196]
  5. ANR [ANR-18-CE15-0011-01]
  6. ENS de Lyon
  7. CNRS
  8. Agence Nationale de la Recherche (ANR) [ANR-18-CE15-0011] Funding Source: Agence Nationale de la Recherche (ANR)

向作者/读者索取更多资源

The gastrointestinal tract contains the enteric nervous system (ENS), which plays a crucial role in controlling motility, fluid balance, and blood flow in the intestine, as well as interacting with other components such as epithelial and immune cells. Recent studies suggest that the diversification of gut microbiota may be essential for the development and function of ENS, potentially starting during fetal development. While the modulation of ENS physiology by microbiota is well-established, further research is needed to fully understand the contribution of gut microbiota to ENS development and pathology, and to uncover the precise mechanisms of microbiota-ENS communication.
The gastrointestinal tract harbors an intrinsic neuronal network, the enteric nervous system (ENS). The ENS controls motility, fluid homeostasis, and blood flow, but also interacts with other components of the intestine such as epithelial and immune cells. Recent studies indicate that gut microbiota diversification, which occurs alongside postnatal ENS maturation, could be critical for the development and function of the ENS. Here we discuss the possibility that this functional relationship starts in utero, whereby the maternal microbiota would prime the developing ENS and shape its physiology. We review ENS/microbiota interactions and their modulation in physiological and pathophysiological contexts. While microbial modulation of the ENS physiology is now well established, further studies are required to understand the contribution of the gut microbiota to the development and pathology of the ENS and to reveal the precise mechanisms underlying microbiota-to-ENS communications.

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